Key result
Doxorubicin administration caused systemic insulin resistance and decreased the expression of key insulin signaling genes, including IRS-1, GLUT4, AMPK, and GSK3b, in skeletal muscle.
p-value: p=<0.05
May warrant metabolic monitoring during doxorubicin therapy; leaves open its contribution to long-term cardiotoxicity or diabetes risk.
Background Doxorubicin is an antibiotic largely used in clinical practice for the treatment of several types of tumors. However, its application may be limited by triggering some host’s deleterious effects, such as extreme fatigue, anorexia, sarcopenia, cardiovascular diseases, among others [1]. The role of skeletal muscle in this process should be further elucidated as this tissue is still important for glucose homeostasis [2] and becomes impaired by doxorubicin treatment. Knowledge of doxorubicin’s effect in the skeletal muscle and in the mechanism of action involved on the systemic insulin sensitivity is still incipient. The aim of this study is to evaluate the mechanism of insulin resistance after doxorubicin treatment.
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Lima et al. (2014) studied Insulin resistance. Doxorubicin vs. Saline was evaluated on Systemic insulin sensitivity and mRNA expression of insulin pathway in skeletal muscle (p=<0.05). Doxorubicin administration caused systemic insulin resistance and decreased the expression of key insulin signaling genes, including IRS-1, GLUT4, AMPK, and GSK3b, in skeletal muscle.
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